scholarly journals Phosphatidylinositol 3-kinase (PI3K) Signaling and Regulation of the Antibody Response

Cell Cycle ◽  
2007 ◽  
Vol 6 (4) ◽  
pp. 397-402 ◽  
Author(s):  
Sidne A. Omori ◽  
Robert C. Rickert
Keyword(s):  
Antibody Response ◽  
Pi3k Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals Phosphatidylinositol 3-Kinase (PI3K) Signaling via Glycogen Synthase Kinase-3 (Gsk-3) Regulates DNA Methylation of Imprinted Loci

2010 ◽  
Vol 285 (53) ◽  
pp. 41337-41347 ◽  
Author(s):  
Anthony P. Popkie ◽  
Leigh C. Zeidner ◽  
Ashley M. Albrecht ◽  
Anthony D'Ippolito ◽  
Sigrid Eckardt ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3 ◽  
Pi3k Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

Ras, Rac1, and phosphatidylinositol-3-kinase (PI3K) signaling in nitric oxide induced endothelial cell migration

Nitric Oxide ◽  
2015 ◽  
Vol 47 ◽  
pp. 40-51 ◽  
Author(s):  
Roberta Eller-Borges ◽  
Wagner L. Batista ◽  
Paulo E. da Costa ◽  
Rita Tokikawa ◽  
Marli F. Curcio ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Endothelial Cell Migration ◽  
Pi3k Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals Hypercholesterolaemic Serum Increases the Permeability of Endothelial Cells through Zonula Occludens-1 with Phosphatidylinositol 3-Kinase Signaling Pathway

2009 ◽  
Vol 2009 ◽  
pp. 1-5 ◽  
Author(s):  
Chang Bian ◽  
Geng Xu ◽  
Jianan Wang ◽  
Ji Ma ◽  
MeiXiang Xiang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Pi3k Signaling ◽  
Dependent Manner ◽  
Phosphatidylinositol 3 Kinase ◽  
Zonula Occludens ◽  
Cultured Endothelial Cells ◽  
Pi3k Signaling Pathway ◽  
Zonula Occludens 1 ◽  
Phosphatidylinositol 3

Purpose. Hypercholesterolemia and tight junctions play important roles in atherosclerosis. But the relationship between these two factors is unclear. In the present study, we investigated whether hypercholesterolemic serum could change the permeability of endothelial cells through altering expression and/or distribution of tight junction protein zonula occludens-1 (ZO-1). Phosphatidylinositol 3-kinase (PI3K) signaling pathway was also examined.Materials and Methods. Cultured endothelial cells were treated with different concentration levels of hypercholesterolemic serum. The expression and distribution of ZO-1, the permeability of cultured cells and the involvement of PI3K signaling pathway were measured by various methods.Results. In the present study, we found that hypercholesterolemic serum could not change the expression of ZO-1 either in mRNA or protein level. However, hypercholesterolemic serum could change the distribution of ZO-1 in cultured endothelial cells, and increase the permeability with a dose-dependent manner. When PI3K specific inhibitor wortmannin was used, the effects induced by hypercholesterolemic serum could be partly reversed. The role of PI3K signaling pathway was further confirmed by PI3K activity assay.Conclusions. Our results suggested that although hypercholesterolemic serum could not change the expression of ZO-1, it could change the distribution and increase the permeability in endothelial cells through PI3K signaling pathway.

scholarly journals The p110α Isoform of Phosphatidylinositol 3-Kinase Is Essential for Polyomavirus Middle T Antigen-Mediated Transformation

2007 ◽  
Vol 81 (13) ◽  
pp. 7069-7076 ◽  
Author(s):  
Tamara Utermark ◽  
Brian S. Schaffhausen ◽  
Thomas M. Roberts ◽  
Jean J. Zhao
Keyword(s):  
Cellular Transformation ◽  
Cell Types ◽  
Pi3k Pathway ◽  
T Antigen ◽  
Pi3k Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Gene Encoding ◽  
Pi3k Activation ◽  
Middle T Antigen ◽  
Phosphatidylinositol 3

ABSTRACT Middle T antigen (MT) of polyomavirus is known to play an important role in virus-mediated cellular transformation. While MT has been extensively examined in spontaneously immortalized rodent fibroblasts, its interactions with cells of other types and species are less well understood. We have undertaken a cross-species and cross-cell-type comparison of MT-induced transformation in cells with genetically defined backgrounds. We tested the transforming abilities of a panel of MT mutants, Y250F, Y315F, and Y322F, that are selectively mutated in the binding sites for the principal effectors of MT—Src homology 2 domain-containing transforming protein, phosphatidylinositol 3-kinase (PI3K), and phospholipase C-γ, respectively—in fibroblasts and epithelial cells of murine or human origin. We found that the Y315F mutation disabled the ability of MT to induce transformation in all cell types and species tested. While Y315F also failed to activate the PI3K pathway in these cells, genetic evidence has indicated Y315 may make other contributions to transformation. To confirm the role of PI3K, the PIK3CA gene, encoding p110α, the prime effector of PI3K signaling downstream from activated growth factor receptors, was genetically ablated. This abolished the transforming activity of MT, demonstrating the essential role for this PI3K isoform in MT-mediated transformation. The Y250F mutant was able to transform the human, but not the murine, cells that were examined. Interestingly, this mutant fully activates the PI3K pathway in human cells but activated PI3K signaling poorly in the murine cells used in the study. This again points to the importance of PI3K activation for transformation and suggests that the mechanism by which MT activates the PI3K pathway differs in different species.

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